**7.4 Formulation of immune response**

In the formulation of immune response, Treg cells a produce homeostasis and secondly the autoimmune suppression. A growing body of evidence suggests that the Treg cell repertoire contains organ-specific/tissue specific Treg cells. Treg cell share specificities in lymph nodes throughout the body, suggesting that the anatomical distribution of Treg cells is shaped by the presentation of regional organspecific antigens [97]. On the other hand, the Macrophages (Mϕ) show profound differences with various profiles. Under the influence of an alternative phenotype (also labeled M2 cells) which occurred by the presence of helminth infection. This is driven by type 2 cytokines IL 4 and IL 13 cytokines (**Figure 3**). Ongoing research divided these Mϕ by gene expression, metabolism, and function differences into classically activated (M1) macrophages. However, M2 macrophages are required in the effective immunity to some parasites (including *H polygyrus*) [15]. The DCs are professional antigen-presenting cells (APCs) that play an essential role in presenting antigen to T cells to initiate immune responses. Although the role of DCs in inducing TH 1, TH 17, and Treg responses is well established. Often overshadowed by their T-cell counterparts, regulatory B (Breg) cells are also crucially important in control of the immune response during helminth infection [15] (**Figure 8**).

These DCs can also patrol among enterocytes while extending dendrites towards the lumen [16]. Treg cell population by producing IL-10 to harness immune tolerance [98]. CX3CR1+ phagocytic cells can capture Salmonella by extending dendrites across epithelium in a CX3CR1-dependent manner [99]. Antigens captured by CX3CR1+ phagocytic cells can be transferred through gap junctions to CD103+ DCs in the lamina propria to establish oral tolerance [100]. In addition to luminal antigen, lamina propria CX3CR1+ cells facilitate the surveillance of circulatory antigens from blood vessels [73].
